Abstract 179P
Background
Exercise training reduces tumour growth by increasing tumour-infiltrating T cell density in preclinical models. However, it remains unknown whether exercise training can modify intratumoural T cells in humans. Objective: To compare the effects of exercise training intervention versus control on human prostate intratumoural T cell density.
Methods
This study is a secondary analysis of a randomised controlled trial. We randomly allocated men (age >18 years) with treatment-naïve localized prostate cancer scheduled to radical prostatectomy 2:1 to exercise training intervention or control. The exercise intervention consisted of supervised, high-intensity interval bicycling four times per week from the time of randomization until prostatectomy. Intratumoural CD3+ and CD8+ T cell densities in diagnostic biopsies and post-surgical prostatectomy specimens were quantified using immunohistochemistry. Between-group differences in changes from baseline to follow-up were estimated using constrained baseline linear mixed-effect models.
Results
A total of 30 participants were included (exercise intervention, n=20; control, n=10). We found no between-group differences in changes in CD3+ (mean difference [95% Cis]: –17 [–185; 150] cells/mm2) or CD8+ (mean difference [95% CI]: –16 [–206;172] cells/mm2) T cells. Additionally, we found no statistically significant correlations between changes in T cell density and the number of attended exercise training sessions or changes in maximal oxygen consumption.
Conclusions
In this secondary analysis of a randomised controlled trial, we found no impact of exercise training on tumour-infiltrating CD3+ and CD8+ T cell density in human prostate cancer.
Clinical trial identification
Local Ethics Committee of the Capital Region of Denmark (H-18020711). All participants provided informed consent before performing any study-related procedures, and the study was preregistered at www.clinicaltrials.gov (NCT03675529).
Legal entity responsible for the study
The authors.
Funding
TrygFonden and the Lundbeck Foundation.
Disclosure
All authors have declared no conflicts of interest.
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